Nicotinic acetylcholine receptor mRNA in dorsal root ganglion neurons

Abstract

Nicotinic acetylcholine receptor (AChR) genes are expressed in subpopulations of chick dorsal root ganglion (DRG) neurons. In 18-day embryonic ganglia, 19% of the neurons have material homologous to neuronal AChR alpha 3 gene mRNA, and 8% have material homologous to alpha 4 mRNA as seen with in situ hybridization. RNAase protection experiments confirm that DRG RNA contains alpha 3 and alpha 4 transcripts, and Northern blot analysis establishes the size of the transcripts as being 3.5 and 3.3 kb, respectively. The proportion of DRG neurons containing alpha 3 mRNA does not decline up through 1 year post-hatch, indicating that alpha 3 gene expression is not a developmentally transient event in the ganglion. An antiAChR monoclonal antibody detects cross-reacting material in 16% of the DRG neurons from 18-day embryos, indicating that AChR mRNA is translated into protein. Electrophysiological measurements confirm the presence of functional AChRs on DRG neurons freshly isolated from 18-day embryos: 24% of the neurons have substantial ACh sensitivities, whereas another 23% have small but detectable responses. Staining dorsal root ganglion sections with an anticholine acetyltransferase antiserum reveals cross-reactive material localized in axons in the ganglion; no evidence suggests the presence of cholinergic synaptic structures or AChR clusters on neuronal somata in the ganglion. It is possible that AChRs on DRG neurons participate in a diffuse form of transmission between the cholinergic fibers and a subpopulation of neuronal somata in the ganglion. Alternatively, AChRs on the somata may represent an ectopic distribution of receptors whose primary function is at the terminals of central or peripheral DRG processes.

Satellite glial cells in sensory ganglia: from form to function

“…Sensory neurons express both types of ACh receptors, nicotinic [19] and muscarinic [17], and display functional responses to ACh, as found both electrophysiologically [70] and by ACh-stimulated NO synthesis [61]. DRG neurons contain the enzyme choline acetyl transferase, which catalyses ACh synthesis [167], and they also express the vesicular acetylcholine transporter, which is required for loading ACh into synaptic vesicles [169].…”

Topical and Peripherally Acting Analgesics

“…However, it now is recognized that peripheral sources of ACh could include sensory neurons themselves (Tata et al, 1994) or keratinocytes and fibroblasts (Grando et al, 1993), and these may release ACh following cutaneous injury. Nicotinic receptors are present on sensory afferent neurons (Boyd et al, 1991;Roberts et al, 1995), and multiple nicotinic receptor subtypes are expressed (Flores et al, 1996;Genzen et al, 2001). ACh can activate sensory afferents through nicotinic receptors (Steen and Reeh, 1993;Jinks and Carstens, 1999;Bernardini et al, 2001), and nicotinic agonists produce sensations of irritation or pain when delivered to skin or the oral mucosa (Dessirier et al, 1997(Dessirier et al, , 1998.…”

Antinociceptive and anti-inflammatory effects of a Geissospermum vellosii stem bark fraction

“…nAChRs are extensively distributed in central nervous system (CNS) and peripheral sites. Although most reports focus on the central sites of the analgesic action of nicotinic agonists (Damaj et al 1998, Khan et al 1994, Sahley and Berntson 1979, α-7 nAChRs were found in peripheral sites, such as ganglion neurons of the dorsal root (Boyd et al 1991, Hu and Li 1997, Genzen et al 2001.…”